Abstract The current proposal takes a circuit-based approach to investigate how the gustatory cortex (GC) processes the hedonic value (or palatability) of a food in cooperation with the basolateral amygdala (BLA) and lateral hypothalamus (LH). This complex circuit approach is taken because the control of ingestion is a complicated process: while physiological needs (e.g., hunger, thirst) exert an important force on consumption, the hedonic value of a taste plays a powerful, potentially competing role; in fact, we often eat or drink not to satisfy physiological needs but to fulfill the desire to consume palatable food?a desire that, in extreme cases, may eventually lead to disorders such as binge eating and bulimia nervosa, severe social issues that affect millions of people a year in the United States. Our work has established that GC, the cortical projection of the central gustatory system, plays a pivotal role in processing the hedonic value of a taste stimulus: GC taste responses show 2 temporally separated firing epochs, the first representing taste identity (here, Epoch 1) and the second epoch reflecting the hedonic value conveyed by the taste (Epoch 2); furthermore, this activity not only reflects palatability but plays a role in causing it?the onset of Epoch 2 predicts the timing of taste-evoked orofacial responses, and inhibition of GC significantly perturbs production of those responses. The current work will extend these findings by exploring the rich reciprocal connections between GC and BLA and LH, subcortical areas in which taste responses also show epoch-like firing activity. I hypothesize that palatability-related firing in GC requires inputs from BLA and/or LH. To test this hypothesis, I will directly examine how optogenetic silencing of projections from BLA and/or LH influence GC taste responses (Aim 1) and learning-related changes in palatability (Aim 2, conditioned taste aversion or CTA). Finally, in Aim 3, with the use of a genetically engineered rat model (ChAT::cre+ rats), I will evaluate the influence of cholinergic signaling perturbation on nave and learning-related palatability behavior and attendant neural responses, thus deepening my search for specific pathways responsible for the processing of palatability. Together, this research project will enrich our understanding of neural control of palatability-mediated consumption, based on which we may identify more effective treatment and prevention strategies for eating disorders.